Look through your standing orders and protocols for the usage of EtCO2. You will probably (hopefully) find ETI or Supraglottic airway confirmation… Do you see anything else? Unfortunately, there are very few services out there that utilize one of the greatest diagnostic tools we have: waveform capnography. So if this is such a great diagnostic tool, which patients should we be using this on? Any trauma, cardiac, respiratory, overdose, arrest, or illness that just has that “sick” look. This is a crash course on capnography and some of the major uses we should be using it for.

ETCO2 AND DETECTING BRONCHOCONSTRICTION

Allow me to paint a clearer picture using a scenario that isn’t altogether too uncommon. You and your partner are dispatched to a mid-70s female patient that is seated in her recliner and obviously dyspneic. You notice the swollen ankles and the array of medications sitting in a bin next to her. As you begin to rifle through the container, the patient, in between breaths, tells you that despite using her rescue inhaler and a nebulizer treatment, she isn’t improving. The patient takes Lasix, Diltiazem, Coumadin, Albuterol, Metoprolol…and the list goes on. By simple deduction, you’ve figured out that the patient has several co-morbidities, including CHF and COPD. So what are you going to treat for? You listen to the patient’s lung sounds and hear coarse wet sounds in the bases, but also hear expiratory wheeze in the upper lobes. Could anything else besides bronchoconstriction create a wheezing sound? Cardiac asthma? If only there was something we could use to differentiate between cardiac asthma and bronchoconstriction…

WAVEFORM CAPNOGRAPHY WITH NO BRONCHOCONSTRICTION

WAVEFORM CAPNOGRAPHY REVEALING BRONCHOCONSTRICTION

ETCO2 AND DETECTING POOR CARDIAC OUTPUT

Okay, so you can use EtCO2 to differentiate between cardiac asthma and COPD exacerbation…big deal. What else can this tell us? Well, I’m glad you asked. EtCO2 is one of the most reliable prehospital indicators of cardiac output. Normal ranges of EtCO2 are typically between 35-45mmHg (although you’ll hear some argument from some saying that there is a slight discrepancy between waveform capnography and actual blood gas CO2 values). As cardiac output decreases, so does your EtCO2. Conversely, as cardiac output increases, so does your EtCO2. EtCO2 is a tool that allows you to monitor a patient’s responsiveness to colloid/blood therapy and pressor resuscitation. It’s time to consider using routine EtCO2 in sepsis, trauma, suspected PE or anyone showing signs and symptoms of shock.

WAVEFORM CAPNOGRAPHY REVEALING POOR CARDIAC OUTPUT

ETCO2 IN TRAUMA

Decompensating trauma patients need to be monitored with EtCO2. A great example of the usefulness in the trauma patient is in the case of tension pneumothorax and cardiac tamponade; due to the increased intrathoracic pressure or fluid in the pericardium, the heart’s ability to perfuse the body is greatly inhibited. EtCO2 monitoring shows in real time, the effectiveness of thoracostomy or cardiocentesis.

What about the head injured patient? The majority of us were taught early on in our EMT-Basic classes to hyperventilate the head-injured patient. We now know that hyperventilating these patients leads to decreased ICP and cerebral blood flow, leading to higher mortality rates. The truth of the matter, is that ventilatory management of these patients is a balancing act, and EtCO2 monitoring is the only reliable indicator that you are keeping the patient from experiencing respiratory alkalosis or acidosis. Improper ventilatory management can be the tipping point between life and death. If we are really honest with ourselves, all of us have experienced at one time or another hyperventilating a patient due to our own stress. By monitoring EtCO2, we have real time data showing us what we need to do for our patients. Try to keep your head injuries between 30-35mmHg.

ETCO2 IN NARCOTIC OVERDOSE

I think all of us are a little too quick to pull the narcan trigger in narcotic overdose. This is a personal opinion, completely. Remember that mild bradypnea does not always mean that the patient is not being ventilated adequately.

CURARE CLEFT

Essentially, the curare cleft is an indicator that your patient is exhibiting spontaneous respiratory effort despite the insertion of an endotracheal tube, supraglottic airway, or surgical airway. The dip in the waveform is essentially the diaphragm of your patient that is “waking up” from deep sedation or the paralytics you have given.

SOAP BOX MINUTE WITH MIKE

There are some realistic limitations to what EMS services can provide to our patients. Financial shortage is a real problem. Lack of education should never be what’s holding your service back, though. I have heard several people say that they are afraid to implement EtCO2 into widespread system usage because it would take too long to train all of their employees into using it correctly. We have a duty to our patients to provide the best care possible under every circumstance. EtCO2 is one of the most reliable diagnostic tools available to the prehospital provider, and we need to be utilizing it to its full potential.

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Thanks for sharing. When you refer to head injury are you refering to isolated head injury or the multi trauma patient. As much as I agree with this statement we must remind ourselves of the correlation between ETC02 and PC02 are only linear in the euvolemic normal cardiac output state. Blood loss and low cardiac output both lead to inverse correlation between ETC02 & PC02, one goes down one goes up respectively. Attempting to correct ETC02 through changing your ventilation strategy in severe blood loss could lead to severe acidosis and increase the ICP exacerbating the head injured patient.

Absolutely, Dan. We should have clarified that this is in the event of isolated head injury. In states of hypovolemia, head injury management becomes increasingly more difficult and MAP is probably your best indicator of treatment without altering your ventilation rate.